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SRC-1 Knockout Exerts No Effect on Amyloid β Deposition in APP/PS1 Mice
Qiong Wu1, Bin Wang1, Qi-Fa Li1
1Liaoning Provincial Key Laboratory of Cerebral Diseases, Department of Physiology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Frontiers in Aging Neuroscience
|July 7, 2020
Summary
Steroid receptor coactivator 1 (SRC-1) deletion did not impact amyloid-beta deposition or synaptic protein levels in Alzheimer's disease (AD) mouse models. This suggests SRC-1 may not play a role in AD pathogenesis, though further research is needed.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Steroid receptor coactivator 1 (SRC-1) is crucial for transcriptional activity and abundant in the hippocampus, influencing cognition.
- SRC-1 is linked to Alzheimer's disease (AD) risk factors like aging and estrogen decline, but its role in AD pathogenesis is unknown.
Purpose of the Study:
- To investigate the role of SRC-1 in Alzheimer's disease (AD) pathogenesis.
- To determine if SRC-1 knockout affects amyloid-beta (Aβ) deposition, synaptic protein expression, or glial activation in an AD mouse model.
Main Methods:
- Established a mouse model by crossing SRC-1 knockout mice (SRC-1-/-) with APP/PS1 transgenic mice to create APP/PS1×SRC-1-/- mice.
- Analyzed hippocampal expression of synaptic proteins, amyloid-beta (Aβ) plaque deposition, and activation of astrocytes and microglia.
Main Results:
- SRC-1 knockout did not alter amyloid-beta (Aβ) plaque deposition in the hippocampus.
- Deletion of SRC-1 did not affect the activation of astrocytes and microglia.
- No significant changes were observed in the expression of synaptic proteins in the APP/PS1×SRC-1-/- mice.
Conclusions:
- Complete embryonic deletion of SRC-1 has no discernible effect on the pathogenesis of APP/PS1 mice.
- This study does not rule out a potential role for SRC-1 in AD development, considering limitations such as the absence of tau hyperphosphorylation analysis and the specific animal model used.
